Activation of Adenylate Cyclase of Rat Ascites Hepatoma by Catecholamines and Antagonism of β-Adrenergic Blocking Agents

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Abstract
Activation of adenylate cyclase [AC] of rat ascites hepatoma, AH-130, AH-272, AH-66 and AH-7974, by catecholamines, glucagon and NaF, and effects of .beta.-adrenergic blocking agents were studied. Basal AC activity of AH-7974 was higher than those of the other 3 tumors as well as of the liver. AH-130 AC was activated by epinephrine and isoproterenol more than that of the liver; those of other tumors showed lower responses to catecholamines. The response of tumor AC to glucagon was very low compared with that of the liver. NaF activated all the tumor AC tested. Activation of AH-130 AC by epinephrine was inhibited by .beta.-adrenergic blocking agents such as bufetolol, practolol, propranolol and alprenolol, but was not blocked by .alpha.-adrenergic blocking agents like phentolamine and phenoxybenzamine, and by antitumor alkylating agents, bis(3-methylsulfonyloxypropyl) amine p-toluene sulfonate and nitrogen mustard. The effect of practolol, a selective .beta.1-adrenergic blocking agent, was less than other 3 agents. Apparently AH-130 possesses a .beta.2-adrenergic receptor coupled with AC and may be useful as a tissue in place of liver for research on .beta.-adrenergic blocking agents.

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